Guo Qian,Guo Jiabin,Yang Rong,Yuan Haitao,Peng Shuangqing,Li Li.Protective effect of cyclovirobuxine D on mice suffered from doxorubicin-induced cardiotoxicity[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(13):1341-1344.
Guo Qian,Guo Jiabin,Yang Rong,Yuan Haitao,Peng Shuangqing,Li Li.Protective effect of cyclovirobuxine D on mice suffered from doxorubicin-induced cardiotoxicity[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(13):1341-1344.DOI:
Protective effect of cyclovirobuxine D on mice suffered from doxorubicin-induced cardiotoxicity
Objective To observe the effect of cyclovirobuxine D (Cvb-D) on mice suffered from doxorubicin (DOX)-induced cardiotoxicity. Methods Adult C57 mice were randomly divided into four groups (n=12) including a control group
a Cvb-D group
a DOX group and a Cvb-D+DOX group. Mice were given Cvb-D (1 mg/kg) intragastrically once a day for 4 consecutive days
followed by a single intraperitoneal injection of DOX (15 mg/kg) or saline
and the body weight was recorded thereafter. Four days later
the serum l
evels of creatine kinase (CK) and lactate dehydrogenase (LDH) and the activity of myocardial caspase-3 were determined
and cardiac tissue sections were stained with Masson’s trichrome to observe the morphology of myocardium. Apoptotic cells in cardiac tissues were observed by TUNEL assay. The protein expression levels of Bcl-2 and Bax were determined by Western blotting
and the ratio of Bcl-2/Bax was calculated. Results Cvb-D administered alone had no obvious effect on mice as compared with the control group. Pretreatment with Cvb-D significantly rescued DOX-induced decrease of body weight in mice (
P
0.05)
and alleviated myocardial fibrosis. Cvb-D significantly inhibited DOX-induced increase in serum levels of LDH and CK and caspase-3 activity (
P
0.05) in cardiac tissues
and relieved DOX-induced myocardial apoptosis. Cvb-D also improved the ratio of Bcl-2/Bax expression decreased by DOX. Conclusion Cvb-D has a protective effect against DOX-induced cardiotoxicity possibly by inhibiting cell apoptosis.
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